Chromium is absorbed from oral, inhalation, or dermal exposure and distributes to nearly all tissues, with the highest concentrations found in kidney and liver. Bone is also a major storage site and may contribute to long-term retention. Hexavalent chromium's similarity to sulfate and chromate allow it to be transported into cells via sulfate transport mechanisms. Inside the cell, hexavalent chromium is reduced first to pentavalent chromium, then to trivalent chromium by many substances including ascorbate, glutathione, and nicotinamide adenine dinucleotide. Chromium is almost entirely excreted with the urine. (A12, L16)
IDENTIFICATION AND USE: Chromic oxide (Cr(2)O(3)) is a green powder. It is not registered for current use in the U.S., but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses. It is used in abrasives and electric semiconductors; in alloys; in printing fabrics and banknotes. It is also used in dyeing polymers; colorant for latex paints, in manufacturing of chromium metal and aluminum-chromium master alloys. It's other uses include catalyst in organic synthesis, green granules in asphalt roofing, component of refractory brick. Chromic oxide is a color additive in drug use. HUMAN EXPOSURE AND TOXICITY: Fine chromic oxide particles were insoluble in the culture medium; on the contrary, Cr(2)O(3) nanoparticles released soluble hexavalent chromium into the culture medium. Human lung carcinoma A549 cells and human keratinocyte HaCaT cells showed an increase in intracellular reactive oxygen species (ROS) level and activation of antioxidant defense systems on exposure to Cr(2)O(3) nanoparticles. The cellular influences of Cr(2)O(3) nanoparticles matched those of hexavalent chromium. Human lung epithelial cells exposure to chromic oxide nanoparticles led to DNA damage, which was detected by comet assay and cytokinesis block micronucleus assay. The cell exposure lead to mitochondria-mediated apoptosis. ANIMAL STUDIES: In rats in a 13-week nose-only inhalation study that included a 13-week recovery period, chromic oxide caused pathological changes in the bronchial and mediastinal lymphatic tissue and lungs, consisting of the presence of pigment-laden macrophages, lymphoid and septal hyperplasia, and interstitial inflammation similar to that observed with other inert dusts. In experiments with rats 4/20 animals developed lung sarcomas 16-19 months after a single intraperitoneal injection of 20 mg chromic oxide. No effects on reproduction were reported in nine pairs of rats fed up to 5% chromium(III) oxide in a supplemented bread, 5 days/week for 60 days before grossly observable malformations or adverse effects occurred in the pups. Exposure to chromic oxide increased sister chromatid exchanges in Chinese hamster V79 cells. Exposure for 18 hr to Cr(2)O(3) induced in Chinese hamster cells a statistically significant increase in the mutation frequency of up to 10-fold over the control. ECOTOXICITY STUDIES: In seeds of Triticum aestivum exposure to 25-100 ug/mL Cr(2)O(3) nanoparticles inhibited the seed germination and seedling growth in concentration dependent manner.
Trivalent chromium may also form complexes with peptides, proteins, and DNA, resulting in DNA-protein crosslinks, DNA strand breaks, DNA-DNA interstrand crosslinks, chromium-DNA adducts, chromosomal aberrations and alterations in cellular signaling pathways. It has been shown to induce carcinogenesis by overstimulating cellular regulatory pathways and increasing peroxide levels by activating certain mitogen-activated protein kinases. It can also cause transcriptional repression by cross-linking histone deacetylase 1-DNA methyltransferase 1 complexes to CYP1A1 promoter chromatin, inhibiting histone modification. Chromium may increase its own toxicity by modifying metal regulatory transcription factor 1, causing the inhibition of zinc-induced metallothionein transcription. (A12, L16, A34, A35, A36)
WEIGHT OF EVIDENCE CHARACTERIZATION: Applying the criteria for evaluating the overall weight of evidence for carcinogenicity to humans outlined in EPA's guidelines for risk assessment (1986), trivalent chromium is most appropriately designated a Group D -- Not classified as to its human carcinogenicity. Using the Proposed Guidelines for Carcinogen Risk Assessment (1996), there are inadequate data to determine the potential carcinogenicity of trivalent chromium ... However, the classification of hexavalent chromium as a known human carcinogen raises a concern for the carcinogenic potential of trivalent chromium. HUMAN CARCINOGENICITY DATA: Occupational exposure to trivalent chromium and other chromium compounds by inhalation has been studied in the chromate manufacturing and ferrochromium industries; however, exposures all include mixed exposures to both Cr(III) and Cr(VI). Cr(VI) species is the likely etiological agent in reports of excess cancer risk in chromium workers. Data addressing exposures to Cr(III) alone are not available and data are inadequate for an evaluation of human carcinogenic potential. ... ANIMAL CARCINOGENICITY DATA: The data from oral and inhalation exposures of animals to trivalent chromium do not support documentation of the carcinogenicity of trivalent chromium. IARC concluded that animal data are inadequate for the evaluation of the carcinogenicity of Cr(III) compounds. Furthermore, although there is sufficient evidence of respiratory carcinogenicity associated with exposure to chromium, the relative contribution of Cr(III), Cr(VI), metallic chromium, or soluble versus insoluble chromium to carcinogenicity cannot be elucidated... /Chromium (III), insoluble salts/
Evaluation: There is inadequate evidence in humans for the carcinogenicity of metallic chromium and of chromium(III) compounds. There is inadequate evidence in experimental animals for the carcinogenicity of metallic chromium, barium chromate and chromium(III) compounds. Overall evaluation: Metallic chromium and chromium(III) compounds are not classifiable as to their carcinogenicity to humans (Group 3). /Metallic chromium and chromium(III) compounds/
The intestinal absorption of trivalent and hexavalent chromium (Cr) given orally (experiment I) or infused in the intestine (experiment II) was investigated in rats. The nonabsorbable form of chromium ((51)Cr2O3) and water-soluble and more absorbable Na2(51)CrO4 (the hexavalent form of Cr) were compared. Total retention of chromium given orally ranged around 15 percent of the dose, regardless of the chromium compounds applied. The absorption rate of chromic oxide, which is considered a nonabsorbable compound, was 14.4 as a percentage of chromium intake. This result indicates that some loss of chromium has to be taken into account in metabolic trials made by the indicator method. In isolated rat intestine, from the injected Cr 2.5% of chromic oxide and 43.2% of sodium chromate were absorbed during an hour (experiment II). The absorbed chromium was transferred to the liver where the liver tissue retained 10.9% of chromic oxide and 51.1% of sodium chromate. Radioactivity of v. cava caudalis following intestinal injection of Na2CrO4 was thirtyfold greater than after Cr2O3 dosing. This phenomenon can be explained by the lower blood clearance of chromate. Different absorption rate of chromate depending on the route of administration could be due to the fact that the hexavalent form given orally was reduced to Cr3+ in the acidic environment of the stomach. When Na2CrO4 was infused directly in the intestine of rats, such reduction could not occur. This means that the acidic gastric juice might play a role in inhibiting the intestinal absorption of Na2CrO4 when this compound is given orally.
In this study, Escherichia coli DH5alpha (ATCC 35218) were exposed to 0-100 ug/mL chromium oxide nanoparticles (Cr2O3, Nps) for 15-120 min to study the internalization of Nps by flowcytometry. A concentration-duration dependent increased side scatter (SSC) confirmed the internalization of Cr2O3 NPs by the E. coli. This study suggests that the uptake of Nps by bacterial cells can be rapidly monitored with flow cytometry for toxicity and risk assessment.
The aim of this study was to find out how marker characteristics could affect digestive transit time in Gallus gallus. One soluble marker, Cr-EDTA, and two insoluble markers, Cr2O3 and chromium-mordanted plant cells of two sizes, were used. Three- to six-week-old chickens were killed in series after the oral administration of the markers at intervals of 0, 0.5, 1, 2, 3, 5, 7, and 9 hr. The amount of chromium in each digestive segment was determined by atomic absorption. There were some differences in the initial distribution of markers; whereas almost the total amount of the chromium-mordanted rice husk of the largest size was found in the crop at time 0, less than half of the Cr-EDTA was found. Marker emptying out of the crop was fast and not related to either the type or size. In contrast, the emptying rate of the gizzard depended on marker particle size. As far as the ceca were concerned, the ileocecal junction allowed the passage of soluble Cr-EDTA whereas solid markers were impeded (Cr2O3) or not allowed to pass through at all (vegetable fiber of any size). It can be concluded that marker selection is of major importance to transit time studies in chickens, since its characteristics can determine transit time in an absolute way.
Small intestinal digestibility can be measured by comparing feed with effluent collected from an ileal T-cannula. Nevertheless, a nondigestible, nonabsorbable marker, such as chromic oxide (Cr2O3), must be included in the diet because simple T-cannula do not divert chyme completely. This study was conducted to evaluate the excretion pattern of Cr2O3 in cannulated dogs because the kinetics of Cr2O3 has not been previously investigated in this nonruminant species. Chromic oxide was added to four diets fed to eight cannulated mixed-breed dogs in a Latin-square design. The four diets contained reciprocal proportions of protein from texturized vegetable protein (0% to 57%) and from beef (100% to 43%), so protein and carbohydrate digestibility varied among diets. All feces were collected during wk 2 and all ileal effluent during wk 3 of each diet period. Ileal recovery of Cr2O3 was almost complete (94%) and was greater than fecal recovery (87%) (P < or =0.03). Recovery was not different among diet groups. Ileal DM digestibility was approximately 2 percentage units lower on d 1 (P < or = 0.007) than on d 2 to 4. Nevertheless, ileal DM digestibility varied little on these subsequent days so single-day collections should be accurate. Chromic oxide concentration in chyme varied widely during each collection but increased at the start and declined towards the end of each collection. Spot sampling may therefore result in inaccurate estimates of nutrient digestibility.
Cr<sub>2</sub>O<sub>3</sub> nanofiber: a high-performance electrocatalyst toward artificial N<sub>2</sub> fixation to NH<sub>3</sub> under ambient conditions
作者：Huitong Du、Xiaoxi Guo、Rong-Mei Kong、Fengli Qu
DOI：10.1039/c8cc07186a
日期：——
Cr2O3 nanofiber acts as a superb electrocatalyst for artificial N2 fixation, showing excellent selectivity and durability under ambient conditions.
Cr2O3纳米纤维在人造N2固定中作为卓越的电催化剂，表现出在常温下优异的选择性和耐久性。
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作者：
DOI：——
日期：——
KROHN K.; HEMME C., LIEBIGS ANN. CHEM., 1979, NO 1, 19-34
作者：KROHN K.、 HEMME C.
DOI：——
日期：——
MOUSSA G. E. M.; BASYOUNI M. N.; SHABAN M. E.; YOUSSEF A. M., J. APPL. CHEM. AND BIOTECHNOL., 1978, 28, NO 12, 875-881
作者：MOUSSA G. E. M.、 BASYOUNI M. N.、 SHABAN M. E.、 YOUSSEF A. M.
DOI：——
日期：——
LYUBOMILOV V. I.; SLESAREVA L. A.; PSHENITSYNA V. P.; SLONIM I. YA.; BULA+, ZH. ORGAN. XIMII, 1979, 15, HO 12, 2450-2456
作者：LYUBOMILOV V. I.、 SLESAREVA L. A.、 PSHENITSYNA V. P.、 SLONIM I. YA.、 BULA+
